One Health - Human, Animal & Environmental Health in Tasmania

Public and environmental health issues in Tasmania is one of the priority areas of the Pollution Information Tasmania, a community group dedicated to investigating and documenting pollution in the state of Tasmania, Australia.

Background to Eco-toxicology studies on Australian marsupials and monotremes
In 2001 Robyn Bolton-Grob from University of Queensland, Jorma Ahokas from RMIT in Victoria and Charles Eason from Manaaki-Whenua Landcare Rereach in New Zealand wrote a comprehensive review chapter on the current level of knowledge about eco-toxicology affecting marsupials and monotremes.

In beginning a section on specific data on marsupial ecotoxicology there is this statement: “Perhaps the most notable finding of this review is simply the lack of information on the exposure of Australian marsupials and monotremes to environmental contaminants”.

There is a tendency to think that because Australia as a vast landmass [7,682,300 square kilometres] with a small human population [22 million], the impact of all human activities on biota is relatively low. In the year from March 1991 to March 1992 the Australian Bureau of Statistics (ABS) identified 4688 tonne of pesticide was purchased and used on 19 million hectares [or 190,000 sq kilometres] of land. That area of pesticide-exposed land represents roughly three times the total land area of Tasmania. Since 1992, there has been an expansion in the conversion of native forests to intensively managed tree plantations and the use of a wide range of biocides [herbicides, fungicides, insecticides and vertebrate poisons]. Ecotoxicology data measuring residues of pesticides in Australia native fauna is continues to be sparse and collected ad hoc. In addition to pesticides and biocides, ABS statistics list at least 3000 to 7000 tonnes of polychlorinated biphenyls (PCBs) that have escaped into the Australian environment. The distribution of these contaminants and duration of usage across the Australian landscape has not been documented and the exposure of native mammals (as well as other vertebrates) is also poorly documented.

As mentioned in other sections listed under Pollution Information Tasmania - Persistent Organic Pollutants in Tasmanian wildlife, biocide residues in marsupials and monotremes have been analysed and documented in only a handful of studies sampling limited numbers of animals from a few species. The most comprehensive investigations of published pesticide residues in Australian wildlife are those conducted by the National Residue Survey(NRS 1989-1997) and the new National Measures Institute (NMI 1997- present). Various reports on specific pesticide residues and persistent organic pollutants have been published. Bolton-Grob et al have tabulated all the published data by species, number, residue type and reference citation for organochlorine and organophosphate residues up to the date of their publication (2001. The principle emphasis of these samplings was in relation to the commercial export trade of harvested kangaroos and possums. In the case of the kangaroo samplings, a random sample from approximately 100 kangaroos per year from all the states harvesting the large free-range kangaroos (Macropus rufus, M. fuliginosus,M. giganteus and M. robustus predominantly) - Queensland, New South Wales, Western Australia, South Australia and Victoria - were analysed for pesticide residues between 1989 and 1997 (n=823); that number represents 0.0032% of the 25,955,853 large kangaroos killed between 1989 and 1997.here (Pdf) Detectible organochlorine (OC) residues were found in only 29 of 823 (3.5%) during the 9 years of these NRS studies. No locational detail is available on whether there were any contributing factors for these detections and it is assumed no prospective follow-up surveys were undertaken on these findings. OCs monitored were total DDT (DDT and its metabolites); chlordane, aldrin, diedrin, heptachlor, lindane, methoxychlor, endosulphan isomers, hexachlorocyclohexane (HCH), hexachlorobenzene (HCB) and polychlorinated biphenyl congeners. The organophosphate(OPs) monitored in the kangaroo samples were bromophos-ethyl, carbophenthion, chlorfenvinphos, chlorpyrifos, chloropyrifos-methyl, coumaphos, diazinon, diclovos, ethion, fenchlorphos, fenthion, fenitrothion, malathion and trichlofon. [Endosulphan and diazinon were detected in an unreported number of kangaroo fat samples at levels of 0.1 mg/kgm or lower].

Similarly in 1996 and 1997 fat samples from 54 brush-tail possums (Trichosurus vulpecula) from Tasmania were tested for the same synthetic pesticides by the NRS, Bolton-Grob and others state that no detectible residues in ‘any brush-tail possum samples’;no citation reference is given to this dataset. In contrast chemical residue data in testicular tissue from 10 male brush-tail possums in another study found total DDT ranged from 0.01 to 0.12 mg/kg; HCB from 0.12 to 0.55 mg/kg; delta-HCH (Lindane) from 0.02 to 0.1mg/kgm and PCBs from 0.12-0.57 mg/kg. There was little difference in residues between urban (Melbourne) and ‘non-urban’ (rural Victorian) possums suggesting that these lipophilic chemicals were ubiquitous in the environment. The PCB levels in these possums were well below the levels detected in Tasmanian platypus. Variation in residue detection levels between studies highlight the possibility of exposure differences between population, localities and species in different parts of the food web.

The only other study measuring contaminant levels in marsupials is a very limited random survey of organochlorine residues in the insectivorous eastern barred bandicoot (Perameles gunnii). The study refers to lipid extracted from liver, kidney or fat tissues from western Victoria; only dieldrin residues are reported [1.29 - 6.52 mg/kg]. Unfortunately this paper does not detail the other OCs and OPs that were tested and presumably not detected. In 1979 pesticide residues in the Australian water rat (Hydromys chrysogaster) from Murrumbidge irrigation area of New South Wales were reported. The analysis of 34 water rats from rice-growing farms reported total DDT levels in livers of between 0.1 and 3.1 ppm DMB; in kidneys of 0.1-1.12 ppm DMB and in mammary tissue of lactating female water rats of 0.28 to 23.75 ppm DMB. The DDT residues were correlated with the broad-scale use of chemical to 'control bloodworm (Chironomus sp) which damages rice seedlings; about 1-4.5 kgm/ha of DDT was applied. The authors concluded that biomagnification of DDT and its metabolites in water rats was as a result of intakes of OC-contaminated fish and crustaceans an to lesser extent small mammals, insects and birds.

Another national dioxin survey was completed in 2004; twenty two kangaroo and wallaby samples were included in the study. In 9 macropod samples analysed had concentrations of PCDD/PCDFs and PCBs that exceeded 1.0 pg TEQDFP/g lipid [range 1.1 - 25 pg TEQDFP/g lipid]. The largest contribution to the TEQ in the kangaroo samples was from PCB congener 126 followed by the penta-polychlorinated dibenzo-p-dioxin [1,2,3,7,8-PeCDD], however, in one western grey kangaroo (Macropus fuliginosus) sample from Para Wirra in South Australia the PCDF congeners contributed more to the toxic equivalence (TEQ) than did PCDDs. Interestingly, 6 western grey kangaroos samples were found to exceed 3 pg TEQ/g fat and thus the maximum level for meat products in Australia. Although these results exceeded the maximum level for meat products, they were set aside because ‘fat content of kangaroo meat is generally low and hence consumption of kangaroo meat is unlikely to contribute substantially to the overall PCDD/PCDF body burden’.ref name="National Dioxin Survey"/> It is noteworthy all but one of the 22 kangaroo samples were collected in 2002 or 2003 when the numbers of kangaroos culled under commercial harvesting quotas was in excess of well in excess of 3 million kangaroos in each year; no samples were submitted from Tasmania despite over 6000 macropods killed under commercial quotas.

The detection on dioxins in commercially registered biocides and widely used in Australia was published in 2010. This new data indicates dioxin impurities in commercial biocides is a neglected source of important bioaccumulated pollutants for the Australian environment. Most of these wildlife toxicology studies took place more than a decade after most organochlorine pesticides and PCBs had been banned. Apart from the targeted sampling of commercially harvested kangaroos, all the other toxicology studies relied on opportunistic samplings of dead animals and the interest of the researchers concerned. These toxicology studies highlight the limited results available on Australian wildlife. The effects of lipophilic xenobiotic chemicals on the health, reproductive success and survival of individual species in Australia remain completely unknown and can only be elucidated through further investigation.

It is notable that the residue concentrations of OC compounds observed in monotremes and marsupials are in the similar range to those reported in human breast milk in Victoria, Australia. Human tissue concentrations and dietary exposure to OC pesticides in Australia have been shown to be greater than that observed in other developed countries. According to Bolton-Grob et al it is difficult to evaluate the impact of persistent organic pollutants or agrochemicals on Australian wildlife, without more thorough surveys. They recommended the urgent need for further sampling of a broad range of native fauna to obtain meaningful environmental contamination data.

Why are Australia’s mammals particularly vulnerable to decline and extinction?
Since European colonisation, Australia has experienced a rate of mammalian extinction that is without parallel on any other continent. A wide range of factors have contributed to the loss in abundance and decline in species richness (biodiversity); they include habitat fragmentation and destruction due to clearing of native vegetation for agriculture, grazing or human development; changes in habitat due to the introduction of exotic weeds, pest and diseases; altered fire regimes and poor land and forest management practices. The geographical and evolutionary isolation of the Australian continent has resulted in an ecosystem and range of species that are highly specialised. It is suggested that Australia’s general aridity, poor soil fertility, topography and rainfall patterns have resulted in ecological landscapes that have little resilience to change. Offshore island ecologies with their geographically-isolated land fauna are particularly susceptible to threats from newly introduced biota and accelerated anthropogenic factors as mentioned above; islands off continents, such as Tasmania, are acknowledged for their own unique endemic biota, and are also important strongholds for several mammals that have declined dramatically since European settlement.

Of particular interest from an Australian ecotoxicological perspective are continual human-induced impacts of habitat fragmentation and the resulting loss of genetic diversity and potential effects of environmental chemicals on ecosystems that are already under considerable environmental stress.

Destruction of natural habitat not only results in a reduction in the extent of available habitat for native species, but also in fragmentation of the remaining habitat into remnants of varying size and degrees of long-term sustainability. A result of habitat fragmentation is subdivision and reduction of the existing fauna populations with the likelihood of local extinctions of some species often occurring and an increase in the abundance of others. The vast amount of habitat fragmentation that the Australlia environment has undergone since European settlement has, without doubt, contributed significantly to the high rate of decline and extinction of a wide range of native mammals and plants.

Despite decades of alerts, the consequences of human-induced habitat fragmentation combined with the use of chemicals in agriculture and forestry activities is only beginning to be considered. Fragmentation of biodiverse habitats into patches surrounded by land conversion for agriculture (pasture, cropping, orchards, vineyards), silviculture (commercial tree plantations) and other forms of land use (industrial or suburban development) can increase the exposure of animals to a range of biocides and industrial chemicals merely through close proximity of wildlife habitat to the sites of chemical use or discharge. In addition, population decline due to habitat fragmentation has been identified as a major source of biodiversity loss. Loss of genetic diversity amongst Australian marsupials that have experienced significant population declines and/or bottleneck due to habitat loss & fragmentation, or other human activities, has been demonstrated.

As previously discussed, many of Australia’s marsupials have evolved and exist in highly specialised ecosystems. Viable self-sustaining populations of some species can only be maintained where strict requirements for habitat - in terms of quality and quantity - are met. Examples of strict ecological specialists are numerous among the Australian marsupial fauna. The low degree of innate flexibility displayed by some species occupying highly specialised ecological niches results in considerable environmental ‘stress’ or ‘dis-ease’. Within a stable forest ecosystem for example, specialist keystone species provide little understood ecological services such as folivores (koala, possums & gliders) and fungivores (bettongs, bandicoots and potoroos).This is highlighted by  the rarity and ongoing vulnerability of these species in the face of human activity. As a result, what may otherwise be considered single, small localised impacts on the ecosystems of these species may, in reality, be catastrophic if it jeopardises one of the essential specialised environmental services that such an ecosystem requires for its long-term sustainability. The risk for environmental chemical exposure to affect every component of a health ecosystem therefore becomes of paramount importance when assessing possible impacts on ecosystems that support highly specialised species. For these reasons, Australia’s co-evolved environment and animals require environmental assessors to be particularly strong advocates in the face of numerous anthropogenic factors acting on ecosystems.

Ways pesticides have gone undetected
When used commercially manufactured, formulations of hexachlorocyclohexane (BHC) consisted of mixtures of at least three main isomeric forms; each with differing biological and toxic properties. The γ isomer, was most concentrated in the formulation Lindane; it was highly toxic for animals and was used extensively because it was the most biological potent against unwanted insects and ectoparasites. The α and γ isomers of BHC in pure formulation caused acute nervous system toxicity characterized by convulsions whilst the β isomer acts as a depressant. The β isomer is poorly metabolized in mammals and is the main BHC chemical residue detected in animal tissues. The variety of ways that persistent organochlorines were used in Australia as biocides to enhance the productivity of broad-acre agriculture, horticultural and silviculture are numerous. The somewhat hidden ways that lindane was used is highlighted by a couple of examples: Lindane was as a ‘seed protectant’ and until at least the early 1990’s was used in Australia to coat rice seed and in the 1970’s and 1980’s lindane was used extensively in superphosphate mixture to control unwanted soil insects of crops and grazed pastures with clinical toxicities detected in grazing livestock due to lindane exposure reported. In one reported incident, the superspreader had failed to function properly and heaped trails of fertilizer containing 1200ppm of lindane were deposited on the soil surface. Lambs grazing the fields after the faulty fertilizer application developed typical nervous signs of acute organochlorine toxicity

Targeted surveillance of ecosystem-scale exposure to persistent organochlorine pesiticides has been pratically non-existent in Australia. In the early 1980’s the New South Wales National Parks & Wildlife Service (NPWS) killed 400 native animals from the north coast region of NSW to determine the extent of OC bioaccumulation by terrestrial fauna. DDT and Dieldrin residues had been consistently detected in livestock meat and cow’s milk from the area since 1969. The project led by Dr Layton Llewellyn was conducted over several years and showed that native birds and mammals were accumulating substantial mean residues of these pesticides [magpies (Gymnorhinia sp.) mean of 1.4 ppm of dieldrin; kookaburras (Dacelo gigas), 0.9 ppm dieldrin & 0.7 ppm total DDT]; most worrying was the mean residues 13 ppm dieldrin and 2.6 ppm total DDT in samplings of ground-feeding bandicoots (Isoodon obesulus and Perameles nasuta).The NPWS study was never published in its final form, however in 1991 the comprehensive residue analyses conducted on soils, river water & sediments and wildlife were released by the North Coast Environment Council. Although the data was frequently referred to in numerous internal NSW government committees, the results remained secret until their release in 1991. In a separate pesticide residue study in the state of Victoria conducted in the late 1980’s, dieldrin residues in insectivorous eastern barred bandicoots (Perameles gunnii) were between 1.29-6.52 ppm (n=5)

Accounts of wildlife declines following pesticide usage
In the real world, animals, like humans, are also subjected to pesticide poisoning. Domestic pets can absorb pesticides from soil in an around chemically-treated houses, and wildlife and farm animals can absorb pesticides through the food web through the leaves, grasses & berries they eat; through soil and river sediments and from drinking the water from water bodies exposed to spray drift. Some animals in the food web accumulate a extra chemical load that comes from being carnivores or carrion scavengers (Tasmanian devils and raptors). In preparing her 1994 book Kate Short received correspondence on wildlife disappearances and deaths. Some organophosphates are quite persistent, for example chlorpyrifos contain 30% by weight chlorine. As a termite-cide used under house foundations, chlorpyrifos can remain active for between 5 and 17 years and in agricultural soil it remains potent for many months; chlorpyrifos has been reportedin Australia domestic water supplies. Chlorpyrifos residues are found in the eggs of pelicans (Pelecanus conspicillatus) and little terns (Sterna albifrons) and recovered from the bodies of dead currawongs (Strepera sp.) in suburban Sydney. The use of chlorpyrifos in urban pest control is considered the only likely source of these wild birds exposure.

Armin Ptak reported ‘the disappearance of native birds from his area’ whilst his farm animals sickened. Ptak lived close by commercial pea farms in South Australia where aerial spray drift was commonly seen and the pesticides smelt in the air; Ptak died of cancer.

Tasmanian Royce Macdonald asked vets to investigate birth defects, lameness and unexplained bleeding in cattle near Exeter in northern Tasmania. The vets diagnosed that animal illness were caused by a toxicosis but were unsuccessful in determining the source, however, soil analysis from his property revealed dieldrin levels so high that Mr Macdonald requested that part of his farm be quarantined. It subsequently was shown that the dieldrin had leached from discarded pesticide drums dumped in a local tip located in a water catchment upstream from Mr Macdonald’s cattle property. This Tasmanian incident is relevant to toxicology studies of platypus and estuarine marine organisms conducted in this part of Tasmania during the same time period.

Pat Jackson of Mungindi in New South Wales reported aerial spray drift from an adjoining cotton farm caused the deaths of cattle and ‘literally thousands of birds, all species. The wild green budgies (Melopsittacus undulatus) which were here in the thousands were completely wiped out.’ ‘In a few years the [cotton] industry has just denuded this fertile area of trees, the river [Barwon River] is dying, the water and birdlife is diminishing at such a rate you can almost hear it happening. They have wiped out colonies of koalas without a second thought. The bees are non-existent'.

Tasmanian platypus and persistent organic pollutants
The role of the bio-accumulated persistent organic pollutants in Tasmania’s platypus — especially the immunogenic and hormone-disrupting synthetic PCBs — need further investigation. There have been surprisingly few studies of residues of persistent organic pollutants in the body tissues of Australia’s unique fauna - the montremes and marsupials. In the late 1990s the first reported residues of polychlorinated biphenyls (PCB) and organochlorine (OC) pesticides in Tasmanian platypus were published. In 1997 Professor Anders Sodergren [University of Lund, Sweden] had a year’s sabbatical in Tasmania. Sodergren worked with Dr Barry Munday from University of Tasmania examining the PCB and OC residues in platypus tail fat. Professor Sodergren was investigating whether there was any link between the mucormycosis skin ulcers in platypus. and chemical pollutants. “Every platypus studied had PCBs, but not all had ulcers. It is very disturbing. Where PCBs were found in platypuses, DDT and other pesticides were also found. This was the original [unmetabolised] DDT and not broken down to components. This means there is either a recent source of DDT or the platypuses were having difficulty breaking down these substances", he said Professor Sodergren could not say what the sources of the PCB residues in the platypus were, however, there was a link with the electricity industry in Tasmania.  "Platypuses are ideal to study because mammals in water are good bioconcentrators. They pick it up easily and find it difficult to release”.

In 2002 considerably higher tail fat residues of PCBs were reported in a platypus associated with a river catchment in which ‘a verified spill of PCBs in transformer oil’ had taken place. This male platypus was sampled on two separate occasions recording 12,340 ppb total PCB (when tail fat reserves represented 38% w/w) and 505,340 ppb (when tail fat reserves were depleted and represented 1.8% w/w).

The total DDT and Lindane levels in 56 Tasmanian platypus were published in 2002 The highest recorded level of ΣDDT was 11,857 ng/g lipid weight (mean of 697 ng/g; SD ± 1747; n=56). These organochlorine residues are among the highest known from any monotremes or marsupial anywhere in Australia. This was somewhat surprising as commercial organochlorine products had been deregistered, for any use, in Tasmania since 1987, therefore residues of pp-DDT recorded in platypus would have necessarily been derived from illegal usage or discharge of retained these chemicals. In a 2001 study by Boulton-Grob and others and covering 982 Australian terrestrial & freshwater animals, residues of the organochlorine, Lindane were only found in Tasmanian devils and platypus from Tasmania.

The literature on PCB residues in platypus has been published in various forms. The 1998 study reported on a survey of nine platypus. with concentrations ranging from 40 to 570 ppb total PCB. In a 2002 study, standardised freeze-dried tail fat from 56 platypus [38 males; 18 females] were analysed for PCB residues. The highest level of total polychlorinated biphenyls was 13,855 ng/g lipid weight (mean of 1201 ng/g; SD ± 3235). Fifty five of the 56 platypus sampled in this study had detectible residues of PCBs and DDT in their tail fat.

The accumulated residues of PCBs in Tasmanian platypus were compared against the concentrations associated with reproductive failure in otters (Lutra lutra) and adverse immunotoxicity affects on the resilience of animals to infectious pathogens. This is particularly relevant to the expression of an ulcerative fungal infection in Tasmanian platypus caused by Mucor amphibiorum. Tasmanian veterinary pathologist, Dr Barry Munday acknowledged that the platypus was a useful freshwater species to monoitor for persistent organic pollutants in that it consumed marcoinvertebrates such as freshwater insect larvae and crustracea and in that respect platypus were comparable to freshwater fish - such as introduced salmonids - more so than to top-order riverine mammals such as otters. ‘If platypus are sampled over an extended period it should be possible to build up a good picture of [POPs] contamination of different regions with lipophilic and bio-available anthropogenic compounds’. Munday recommended ‘top-order predators such as water rats (Hydromys chrysogaster) and humans consuming significant numbers of fish from Tasmania’s northern and north-western river systems’ should be assessed for PCB residues. In national survey of persistent organic pollutants the only samples from Tasmania where 9 fat samples from stranded whales, two platypus and an echidna collected and submitted by UTAS researchers. Astonishingly, Tasmania with its abundance of wildlife and an economy reliant on sea fisheries, aquaculture, game meats and haven for recreational fishers and shooters did not contribute a single wallaby, a duck, a freshwater fish, or a possum as part of this national surveillance of environmental chemical residues!

According to the 2004 dioxins survey of Australian wildlife, the ‘outstanding result’ in a monotreme was a single echidna (Tachyglossus aculeatus) from South Australia which had a total polychlorinated dibenzo-p-dioxins [PCDDs] of over 14 ppb, however, PCB residues reported from the tail fat sample of Tasmanian platypus (another monotreme) has recorded levels one or two orders of magnitude higher than this single South Australian echidna.

In 1997 detection of PCBs in the aquatic platypus was cause for additional for Professor Sodergren. “It is now very important to find out if fish contain these compounds, especially those going into human consumption", he said.

Likely sources of PCB contamination for platypus - forensic toxicology
In a University of Tasmania Bachelor of Applied Science honours thesis by Niall Stewart, PCB and OC residues from 44 platypus were assessed against river catchments and the principle human activities in those regions. The mean total PCB concentration in tailfat lipid was 1118 ppb ± 3067 ppb with the highest recorded residue of 17,335 ppb; mean total DDT concentration was 588 ppb ± 1916 ppb with the highest recorded residue of 13,754 ppb; mean total Lindane concentration was 24 ppb ± 131 ppb with the highest recorded residue of 964 ppb. IUPAC Congener patterns or profiles of the PCB residues were also compared for platypus within regional water catchments in an attempt to determine any relationships with products containing PCBs used in Tasmania. At three of the 5 regions (northwest Tasmania, central north Tamania and the Derwent valley)the PCB congener profiles were similar to those of both Aroclor 1254 and Clophen A50. At a fourth site - Lake Pedder in the south west Tasmania - the profile was also consistent with transformer oil contamination. There is now growing evidence of significant industrial pollution with PCBs in central north Tasmania. and several historical observations that transformer oils were used in earlier decades in Tasmania to ‘settle dust on [dirt] roads'.

The PCB levels at the artificial hydro-electric impoundment dam called Lake Pedder were explained by the proximity of the sampled platypus to the hydro-electric development village of Strathgordon and the diagnostic PCB congener profile was also recovered from platypus in another catchment heavily modified by hydro-electric installations in northern Tasmania (Poatina-Cressy). The high concentrations of DDT, its metabolites and OC Lindane were related to the intensity of agricultural activity; the elevated PCB levels were mainly found in platypus sampled from zones with industrial and hydroelectric developments.

Munday and his colleagues came to the same conclusion - the presence of high levels of PCBs in platypus tail fat was ‘probably related to industrial and electricity generation activities’ in the water catchments inhabited by platypus. They referred to compelling evidence of significant industrial pollution with PCBs in central northern Tasmania and a history of heavy industry involved in pulp, paper and pigment production in northwest Tasmania as well as numerous hydro-electric plants which used transformer oils rich in PCB congeners. Fat from platypus sampled from northwest, central north and central southern Tasmania had bioaccumulated PCB residues in congener proportions closely resembling congener patterns of two commonly used commercial transformer oils (Aroclor 1254; Clophen A50). The high levels of PCBs at a large hydro-electric dam - Lake Pedder - although located in ‘a remote and apparently pristine part of Tasmania’ was a surprise to the researchers ; its proximity to the hydro-electric industrial facility and village was acknowledged. Once again the reported PCB residues in the Tasmanian platypus were considerably higher that the levels detected in 833 analyses of tissues from mainland Australian marsupials ; the highest recorded being 570 ppb in a brush-tail possum (Trichosurus vulpecula).

Oiling Tasmanian dirt roads - an adopted practice
'Oiling' Tasmanian dirt roads using transformer oils containing the highly toxic polychlorinated biphenyls was publicly reported in 2004. The practice of using PCB-rich oils as a dust suppressant was first used in the United States, and in the 1980's, 1990’s and early 2000’s US authorities have been forced to decontaminate soils from sites contaminated with PCBs. A Tasmanian government spokesperson confirmed the same oiling practice was used by Tasmanian government business enterprises involved in roading for dam building. PCBs were used legally in Tasmania until 1987.

'It was the smell of summer in Tasmania. A freshlu oiled dirt road, steaming under the midday sun. For some this acrid oily stench is a childhood memory as vivid as yesterday. A roading truck would spray oily muck and the dry dust roads wouls soak it up like a nappy. The sodden road would stink for weeks. It did the job. Road dust would not blow in the wind, the goo weighted it down. By winter the glug would be washed away and the road needed doing again, next summer’. As mentioned above a statewide study of persistent organic pollutants in the tail fat of platypus by Anders Sondergren, Barry Munday and Niall Stewart found high levels of several PCB congeners. The platypus sampled from the artifical impoundment lake - Lake Pedder - were contaminated with high PCB concentrations. A long dirt road into the original construction village [now called Strathgordon] was built for constrution of the dam and hydroelectricity installations; the road skirts the lake for many kilometres and the platypus researchers concluded that the practice of using spent transformer oils on dirt roads was the most plausible explanation for the platypus PCB contaminations. According to a member of working on the National PCB management plan, Peter Brotherton the practice of discarding waste PCB-rich lubricants and oils into the environment was probably common practice Australia-wide.

In 2004 the Hydro Electric Commission (HEC) of Tasmania had 190,000 litres of PCB contaminated transformer oil still in service but this was destined to be phased out under a National PCB management plan. According to the environment and sustainability manager with the HEC, Andrew Scanlon contaminated transformer oils containing PCBs were burnt at high temperature at the then oil-fired power station at Bell Bay in northern Tasmania.

Of the 30,000 tonnes of PCBs imported into Australia up to 1975, half is unaccounted for. In Tasmania the HEC has been using, storing and transporting PCBs in the remote mountainous areas where hydroelectricity facilities were built. It is understandable that Tasmania adopted the pratice of oiling roads with waste transformer oils as Bevilacqua reports that the United States Council for Science and Health issued statements that the dumping of PCBs into waterways or into soil was acceptable and this practice went on for 70 years.

The Tasmanian government refused to test samples from dirt roads for PCBs even after several former road workers reported the practice of ‘oiling’ dirt roads with spent transformer oils occurred up to the late 1980’s. Dr Niall Stewart, a Tasmanian scientist warned that PCBs profiles recovered from platypus in Tasmania correlated with commercial formulations of transformer oils used by the HEC and that there was other historical information that confirmed these oils were sprayed onto Tasmanian roads. PCBs were used in Tasmania until 1987, ten years after they were banned in the United States, Canada and Europe. A Tasmanian Government spokesperson released a statement saying: ‘In the absence of any evidence to suggest there were PCBs used on Tasmanian roads, or that there is any risk to the environment, the state Government does not have any plans for [PCB] testing at this stage.

Background timeline
The first public report that the Tasmanian Government was intending to test for toxins, synthetic chemicals and pollutants in Tasmanian devils was reported three years ago in January 2005. It was noted that a pilot survey to test the range of potentially damaging chemicals to which wild devils might be environmentally exposed was being drawn up and reviewed. Up to 20 specific poisons, persistent organic pollutants, environmental contaminants and heavy metals were under consideration. The Tasmanian government to this pilot survey to assess any causal association with the spreading devil facial tumour disease (DFTD). Tissues samples were derived from 16 devils (8 DFTD affected and 8 unaffected) were tested for a range of persistent organic pollutants (furans, dioxins, PCB and PDBE congeners and organochlorines).

Before this study commenced a Commonwealth Government toxicological study reported that 8 randomly sampled wild Tasmanian devils had detectable levels of a new group of persistent organic pollutants, the polybrominated biphenyl ethers (PBDEs). At the time the toxicologist in charge of the Commonwealth Government’s organic pollutants analysis unit, Dr Bob Symons said they hadn’t expected the findings in the devils to be so high. “It was a complete surprise to us. We always thought Tasmania was a pretty pristine place, but a result like this shows how far these chemicals can reach and how quickly they can build up in the environment.” Dr Symon’s said the findings showed Australian levels of the United Nations-listed persistent organic pollutant were higher than levels in Europe, where some PBDEs are banned.

Dr Mariann Lloyd-Smith co-ordinator of International Persistent Organic Pollutants Elimination Network was also surprised. 'We are surprised at these levels of this product being found in an animal that lives in remote and reasonably pristine areas. It certainly highlights the dangers of these sorts of polybrominated diphenyl ethers (PBDEs) and the fact that they can travel vast distances (via the atmosphere). They are significant developmental and reproductive toxins and have been related to a range of nasty issues in animal and human health...Of particular concern would be women of child-bearing age or pregnant women. They (PBDEs) can impact on the immune system. They can affect the way the brain develops, the way we think and feel.'

Of somewhat more interest perhaps was the high levels found in a small sampling of Tasmanian farmed salmonids. Three fillet samples of sea-cage Tasmanian Atlantic salmon (11-34 ppb) and in one fillet from a farmed Rainbow Trout (8 ppb). The levels reported to be double the highest PBDEs residue levels detected in a recent study of Great Lakes salmon in North America.

The Tasmanian Government engaged in a preliminary review of the scope & budget for this toxicological review in late 2005. According to the FOI document’s the first tender-costing was provided by National Measurements Institute in December 2005.

In October 2005 an important feature article on the Devil Facial Tumour Disease appeared in The Australian Magazine. The journalist, Matthew Denholm quoted senior DPIW veterinary pathologist, Dr Stephen Pyecroft again stating that this pilot toxicological study was to take place. In the same article two Department scientists raised concerns that the facial cancer could have been begun after Tasmanian devils had been exposed to organophosphate pesticides used in Tasmania.

Key scientists now believe that chemicals used by farmers or foresters triggered the disease [DFTD]. “That’s very likely: that in the first instance, the devil was for some reason or other exposed to a carcinogenic chemical,” Dr Anne Maree Pearse said. There is no shortage of potential chemical culprits. “Take your pick," said Pearse. "Organophosphates can cause genetic damage.”

Nick Mooney, a respected government wildlife biologist instrumental in getting DFTD taken seriously, agrees. Like Pearse, he is a key DFTD team member, and says the exposure of a lone devil, or a small group of devils, to chemicals was the most likely trigger. ''“That’s the likely scenario - that there isn’t ‘a’ chemical to blame, such as organophosphates,” Mooney says. “And if that’s the case it will produce a very interesting public debate with some serious repercussions.”''

In May 2007 residues of Dioxins, PCB congeners, Furans and PBDE congeners in tissue fat samples were analysed by the National Measurement Institute (Australian Government Analytical Labs, Pymble, NSW). The organochlorines & metabolites in fat samples were performed by Analytical Services Tasmania - a UTAS/DPIW analytical facility.

In early 2008 the Tasmanian correspondent for The Australian newspaper received comprehensive datasets of toxicology data on wild Tasmanian devils; these documents were released under Freedom of Information legislation. Toxicology tests revealed 'high' levels of hexabromobiphenyl ether and 'reasonably high' levels of decabromobiphenyl ether- chemicals used to treat electronics, textiles, and furniture.

According to The Australian, analysis of devil fat samples by the National Measurement Institute found what it described as 'high' levels of hexabromobiphenyl (BB153) and 'reasonably high' levels of decabromodiphenyl ether (BDE209). Commercial decabromobiphenyl ether appears to be identical to the BDE209 found in the Tasmanian devils. It is a technical mixture of different PBDE congeners, with PBDE congener number 209 (decabromodiphenyl ether) and nonabromodiphenyl ether being the most common. The term decaBDE alone refers to only decabromodiphenyl ether, the single 'fully brominated' PBDE. It has been argued that this form of flame retardant was safe to replace others because it did not bioaccumulate. (weblink here)

Results
Results on 16 devils (8 DFTD-affected and 8 unaffected) - five were selected from locations in central northern Tasmania (none from the presumed DFDT site of origin in the north-east); 3 from the central highlands; 7 from the south-east and only 1 from the far north-west - were available in September 2007.

The most significant chemical residue detected were the polychlorinated biphenyls (PCBs), the dioxins, the polychlorinated dibenzofurans and polybrominated diphenyl ethers (PBDEs). For the purposes of a quick analysis, I have graphed the detectable POPs for each devil (male and female) aggregated according to geographic region and expressed as the World Health Organisation - Toxic Equivalence for all measured dioxins, furans & PCBs [WHO-TEQDFP]. and the sum of all PBDE congeners (ΣPBDEs).

Despite the very small sampling, it is noteworthy that two devils from the northern region (Beaconsfield & Deloraine) had the highest recorded ΣPBDE levels - i.e. 55 and 28 ppb in their body fat respectively; another devil from Richmond had 13 ppb of total PBDEs.

The highest residues for the PCBs, Furans and Dioxins - expressed as WHO-TEQDFP - were found in a devil from Dunalley in southern Tasmania (15 ppb) whilst two male devils from Marrawah and Dilston each had 8 ppb of these POPs.

Like many top-order predators, Tasmanian Devils have the potential to bioaccumulate over their lifetime certain POPs through carrion feeding. Devils are opportunistic scavengers of any animal carcase; they also would actively predate sick or weakened wildlife, feral animals or domestic animals.

Two commissioned assessment reports were prepared.

“Tasmanian devils are known to be prone to the development of various cancers. This accounts for the relatively tardy identification of the facial cancer. It might be argued that this might make the Tasmanian Devil especially susceptible to chemical carcinogenesis at relatively low concentrations of any suspect compound. As things stand at present no such carcinogen has been identified at a concentration approaching that likely to be carcinogenic. However the propensity for devils to develop cancer is suggestive of potential genetic origins and the potential for some chemical to act on oncogenes in this species. This view is however speculative and unsupported by any of the chemical measurements made to date."

"In the understanding of the natural history of this disease there is a need to keep an open mind on its genesis whether it be mono- or multi-factorial. My opinion is that a primary chemical aetiology is unlikely. Chemical exposure may contribute to disease development but no evidence, as yet provided, would identify any one compound likely to fit this role. It is my view that the possibility of a chemical exposure contribution cannot be totally excluded but that the pattern of disease would suggest otherwise and that the causative factor(s) should be sought elsewhere such as in the direct transfer of cell by bite, already enunciated."

“In summary, I believe the “dioxin” levels in the current devil study are unlikely to be related to the cause or progression of Devil Facial Tumour Disease. However, as “dioxin” data are limited, these results are likely to be of interest to those concerned with ecological and human health risk assessment in Tasmania and elsewhere.”

Dr Tony Ross commenting on his report agreed chemical exposure could not be ruled out in relation tom DFTD. “You can’t rule out chemicals in playing a role in the index case - the first case - and neither can you rule it in,” Dr Ross said.

"In the understanding of the natural history of this disease there is a need to keep an open mind on its genesis whether it be mono- or multi-factorial. My opinion is that a primary chemical aetiology is unlikely. Chemical exposure may contribute to disease development but no evidence, as yet provided, would identify any one compound likely to fit this role. It is my view that the possibility of a chemical exposure contribution cannot be totally excluded but that the pattern of disease would suggest otherwise and that the causative factor(s) should be sought elsewhere such as in the direct transfer of cell by bite, already enunciated."

“In summary, I believe the “dioxin” levels in the current devil study are unlikely to be related to the cause or progression of Devil Facial Tumour Disease. However, as “dioxin” data are limited, these results are likely to be of interest to those concerned with ecological and human health risk assessment in Tasmania and elsewhere.”

Dr Tony Ross commenting on his report agreed chemical exposure could not be ruled out in relation tom DFTD. “You can’t rule out chemicals in playing a role in the index case - the first case - and neither can you rule it in,” Dr Ross said.

Graphical representations of the persistent organic pollutants (Toxic Equivalents for PCB, Dioxin and Furan congeners; PBDE congeners etc) recovered from the fat 16 Tasmanian devils is available here (Pdf).

While Tasmanian devils capacity to bioaccumulate some persistent organic pollutants into their fat tissues should not be unexpected given they are a carrion-feeding carnivore, veterinary pathologist David Obendorf is concerned that inadequate wildlife, food and environmental toxicological sampling in Tasmania might have serious implications for the future of Tasmania’s lucrative aquaculture, dairy and meat industries.


 * “Of somewhat more interest perhaps [than devils] were the high levels found in a small sampling of Tasmanian farmed salmonids. The reported levels in three fillet samples of sea-cage Tasmanian Atlantic salmon, and one fillet from a farmed rainbow trout, were double the highest PBDE residue levels detected in a recent study of North America’s Great Lakes fish,” Dr Obendorf said.

Dr Obendorf added the presence of POPs in devils alone does not confirm a causal association with DFTD, but he believes the detection is disturbing nevertheless, and is concerned both by the omission of devils from the presumed original site of the index cases of DFTD from the sampling, and the apparent lack of priority given to the investigation by the Tasmanian government.


 * “Despite calls from Tasmanian Greens parliamentarians for the study to proceed, there was np progression in the toxicological study throughout 2006, despite the priority of this particular field of investigation being identified in numerous public documents and newsletters prepared by the Tasmanian government DFTD program. The absence of detectible residues of triazines, organophosphates and Compound 1080 is not unexpected, given the tendency of these chemicals to not accumulate in tissues post exposure, but the fact that a range of POPs have also been detected in the fat samples from Tasmanian platypus, another animal that is experiencing an unusual disease pathobiology, such be a cause for concern,” Dr Obendorf said.

Hamish McCallum, professor of wildlife research at the University of Tasmania, said it's unlikely the chemicals caused the devils' disease.


 * 'It's a really, really strange tumor. All the tumor cells in all the devils are essentially a clone—they are all derived from one individual. The event that caused that original mutation to malignancy will never be known. It happened a minimum of ten years ago, and in terms of managing the disease, it's essentially irrelevant. It's not beyond the bounds of possibility that [PBDEs] may suppress the devils' immune systems in such a way that it makes them more likely to develop the cancer.'

Professor McCallum believes devils with high PBDE residues in their fat could have easily ingested biphenyls directly.


 * 'Throughout Tasmania … people maintain outdoor dumps. If somebody chucked a wallaby carcass on top of say, a foam mattress, then … the devils might actually consume quite large quantities of that foam.'

Another Published Report on PBDEs and PBBs in Tasmanian Devils
The manufacture of Poly-Brominated Biphenyls (PBBs) ceased in the United States of America in 1976 after public exposure and concern mainly related to public health exposures resulting from an agriculture contamination episode that occurred in Michigan in 1973–1974.

PBBs were never manufactured in Australia, and according to Australian Government inventory data they were never imported into Australia in the technical grade form, as industrial chemicals. That said, it is almost certain that they entered Australia incorporated in other tradable chemicals and commercial articles.

Polybrominated biphenyls have been used as fire retardants in textile, electronic equipment, and plastics. Mixtures with three different degrees of bromination have been produced en mass and commercially marketed. Technical hexabromobiphenyl (THBB), which has a bromine content of 76%, was mainly used in the United States of America. In Europe, usage of technical octabromobiphenyl (TOBB, 81% bromine) and/or technical decabromobiphenyl (TDBB; 85%, bromine) played a larger role.

Analyses of PBB and PBDE residues in the fat of 16 devils was published in 2009 This paper compared the residue analyses conducted at the Australian National Measurement Institute with data obtained separately in the Institute of Food Chemistry at the University of Hohenheim in Stuttgart Germany using paired devil samples.

PBB congener 153 was the dominating PBB in all samples, and generally contributed with >90% to sum-PBBs. In addition, PBB 138 and PBB 132 were the second and third most relevant congeners but their quantitites were approximately two orders of magnitude lower than PBB 153. By contrast, PBB 154 and PBB 155 were only found at very low amounts in a few of the samples. PBB 154 and PBB 155 congeners are signature indicators for the existence of  octabromobiphenyl (TOBB) or the decabromobiphenyls (TDBB). Their virtual absence in the Tasmanian devil samples demonstrates that PBB residues almost exclusively originate from the previous use of the technical grade hexabromobiphenyl (THBB). This forensic deduction is also supported by the detection of two other PBB congeners - PBB 132 and PBB 138 - both of which are minor congeners of technical grade hexabromobiphenyl. On the other hand, PBB 149 and PBB 167 which are both present in low concentrations in THBB were not detected in the Tasmanian devils, most likely due to the fast transformation of these congeners in the environment.

Evaluation of results: All devil samples contained PBB and PBDE residues. There was no statistical difference in the PBB burden of healthy (n=8) and facial tumour-affected animals (n=8). The mean value was higher in healthy animals (2,790 compared to 1,650 pg/g of lipid), the median value was lower in healthy animals (1040 compared to 1210 pg/g of lipid). The concentrations were higher than PBB concentrations in adipose tissue from the Spanish human population, reported with a range from 160–600 pg/g of lipids, mean value 360 pg/g of lipid. By contrast, PBB residues in marine killer whales (Oricinus orca) from the north-eastern Pacific coast ranged from 3,100-31, 000 pg/g lipids and in bird liver from Japan ranged from 2,000–34,000 pg/g of lipid. Compared to these PBB residue studies of human, killer whale and cormorants samples the concentrations detected in the Tasmanian devils were considered remarkable firstly because PBBs were never manufactured in Australia and secondly because the Tasmanian devils were considered to be feeding at a lower trophic level compared to top predators killer whale and cormorants. In a further study of fish collected from the five Great Lakes of North America, residues of the PBB congener 153 ranged from 4,600–18,900 pg/g of lipid. Moreover, in all these studies, concentrations of PBBs were one or two orders of magnitude lower than the concentrations of PBDEs recorded, whereas in this Tasmanian devil study the ratio of ΣPBBs to ΣPBDEs was up to one order of magnitude higher.

PBDE residues in human breast milk of Australian women
Based on a sampling of 157 breast milks from across Australia, including a sample of 9 from northern Tasmania). The total levels of PBDEs varied by a factor of 3.1 from a minimum of 6.0 ng/g lipid detected in the Tasmanian sample to a maximum of 18.7 ng/g lipid detected in the rural NSW sample. The lowest sum PBDE concentrations (ng g-1 lipid) were found in samples from Tasmania (6.0), Darwin (7.9), rural Victoria (8.2), Hunter (8.6) and Sydney B (8.5). The highest total PBDE concentrations (ng/g lipid) were found in samples collected from rural NSW (18.7), South Australia B (16.3), Western Australia (13.4) and Wollongong (13.3).

Routes of exposure for PBDE compounds have been variously reported to be via dietary exposure, particularly of fish; inhalation of dust containing chemicals that have been mobilized by human intervention; dermal exposure; and occupational exposure.

Only one case of accidental exposure has been reported in the literature. Thus, occupationally exposed groups may include individuals who work in repair, maintenance or dismantling roles in the electronics or computer industries.

PBDE are not manufacted in Australia and it appears there is ignorance about the exact sources and types of PBDE contained in commercial saleable products in Australia. From the results of this Australian 2002 breast milk study, it appears that a significant proportion of PBDE residues are in the form of penta-BDE congeners. It has been recommended that further investigation of the Australian milk samples should include analysis of individual samples to determine more precisely the product sources of these PBDES found in breast milks.

Overall the levels of PBDE congeners reported in Australian breast milk in the 2005 study (11ng/g; n=157) are lower than those reported from USA (29.2ng/g; n=47) and Canada(22.2ng/g; n=20) and higher than in Sweden (1.84 ng/; n=15) and Japan (0.93ng/g; n=6). Variability, both in congener profiles and/or concentration of residues between individual samples, was seen in the Australian breast milk study and has been previously observed in other country-wide samplings; this is a feature not seen with the residues of other persistent organic pollutants (POPs) such as the polychlorinated biphenyls, dioxins and furans.

Tasmanian road workers and the toxic aftermath
‘A Tasmanian government investigation found exposure to bitumen can cause health problems but there was not enough evidence to support a link between bitumen and cancer’.

The Department of Infrastructure identified 156 former bitumen workers in Tasmania, 63 [40%] had died. Workers identified also working with creosote - a known carcinogen to treat timber bridge decking and other road maintenance workers identified working with herbicides along roadsides without adequate protection. Paradoxically the report stated there was no link between exposure to bitumen and cancer, yet then concluded ‘given the presence of carcinogens in refined bitumen fumes, the evidence of carcinogenicity in animals and the known acute irritative effects of bitumen fumes, it remains important that exposure to bitumen fumes is kept as low as practical…'. ‘The most significant concern about long-term health problems is the question of carcinogenicity, particularly in relation to lung cancer and other cancers of the respiratory tract. Absorption of volatile carcinogenic compounds potentially contribute to cancer affecting other body systems, e.g. leukaemia. There is also the question as to whether long-term exposure causes lower respiratory tract irritation contributing to chronic bronchitis.’

Road worker, Frank Manley (aged 75) recalls spraying coal tar waste from the Hobart gasworks onto Tasmanian roads. Forty-four gallon drums of coal tar was poured into the sprayer trucks that spread the coal tar onto road throughout southern Tasmania in the 1960’s. The Tasmanian Government disputes Mr Manley’s recollections since they believe the use of coal tar stopped in 1949. Coal tar is recognised as a potent carcinogen by the International Agency for Research on Cancer (IARC). Investigative journalist, Simon Bevilacqua met former Tasmanian road gangers who were counting up their fallen workmates. Every summer for decades road gangers sealed Tasmania’s roads with bitumen. Laying bitumen during the 1960’s, 70’s and 80’s; many died prematurely of cancers (lung, skin, colorectal and blood cancers) and those still living have other illnesses such as skin conditions and Parkinson’s disease. The men were occupationally exposed to the toxic fumes emitted from the cooking vats of bitumen. Scribbled in the back of a tattered exercise book owned by road worker, Dennis Bone (aged 62) are the names of 35 fellow road gangers; all are now dead. They began dying in the 1970’s; 10 workers died aged in their 40’s, the others survived into their 50’s and 60’s died of cancer. ‘There are more…’ says Dennis Bone. Mr Bone recalls using an axe to cut into the rock-hard bitumen before loading it into ‘kettles’ with flux oils (a mixture of diesel with various additives). The kettles were heated to 350C. In cold weather conditions the additive known as No Strip was added to make the bitumen slurry stickier and slowing its setting time. Drums of powdered recycled tyre rubber and latex were also incorporated into the heated bitumen mixes. According to the former road gangers the men were obliged to stir the heated mixes in the kettles with spades which emitted clouds of fumes and black mist as it cooked. ‘Sometimes you couldn’t see who you were working with’, Mr Bone said. This was the way the bitumen was brewed up in Tasmania during the 1960’s and 70’s with pre-mix asphalts superseding it by the 1980’s. The field teams camped out on the roads, getting the wood to fire the kettles and cooking up the bitumen mixes. The liquefied steaming 'road gang gumbo' was poured into trucks to spray onto the roads. Frank Manley was a spray truck driver for 13 years. He remembers spraying roads with the hot mixes of 60/40 flux oil and bitumen base. Sometimes the gangers used various mixtures of available oils to settle the dust on dirt roads. Blue metal gravel also primed with oil and layers of bitumen were added to sealed roads. Gangers also used hand sprays for part of the road that the truck could not spray. The men wore no protective clothing and at day’s end they were drenched in black sludge.

The Tasmanian Government Report identified some of the bitumen additives as Megamine BA HPR, Preomine, Gilsabind and Redicote 422/60 (No Strip). The report identified that the road workers also used herbicides to clear weeds from road verges - Butoxone 80, 2,4-D, 2,4,5-T (phenoxy-herbicides), ‘Vorox’, ‘Cyndan’, ‘Brush-off’ and the glyphosate-based ‘Round-Up'. Road workers also used old transformer oils rich in PCBs from the state government Hydro Electric Commission (HEC). Road workers reported using these waste transformer oils in their sprayer trucks to settle dust on dirt roads and as a primer before bitumen was laid.

‘There’s too many of us dead. I’ve been saying this for years’, Mr Bone said. ‘Most of us have got something wrong, if we’re not dead’, Mr Manley said. 'There’s skin rashes, dermatosis, lung problems, things they [doctors] can’t say what it is.’ Mr Manley has hands and arms covered in flaky skin; Mr Bone has been diagnosed with diabetes and Parkinson’s disease.'It was a bastard of a job, sucking in all these fumes into you' said Frank Manley. 'If anything was going to kill you it was this stuff' Dennis Bone recalls about 'No Strip', an additive to the bitumen brew used by Tasmanian road workers.

Chemicals and Cancer - 2010 Report
The UK CHEM Trust have just released their report entitled: A review of the role pesticides play in some cancers: Children, farmers and pesticide users at risk? pdf here. The Chemicals, Health and Environment Monitoring Trust is a UK-based NGO committed to protecting human health and wildlife from harmful chemicals. Their report provides a summary of the epidemiological and related data linking exposure to pesticides with certain cancers. It examines the links between exposure to pesticides and the occurrences of Non-Hodgkins Lymphoma (NHL), soft tissue sarcoma, leukaemia, prostate cancer and brain cancer among other cancers. The report then considers the policy and regulatory responses that are needed and concludes with pertinent recommendations; it has direct relevance for other justidictions, including Tasmania.

List of Australia's most dangerous pesticides
In July 2010 World Wildlife Fund Australia and National Toxics Network released a comprehensive list of Australia’s most dangerous pesticides. Over 8000 pesticide and veterinary products are registered for use in Australian agriculture, horticulture, livestock, forestry, commercial premises, parks, homes and gardens; more than 80 are prohibited in the European Union. Australia does not have the same system as Europe and our national regulator, the Australian Pesticides and Veterinary Medicines Authority (APVMA) does not apply the same precautionary approach. This list also includes 17 pesticides that are known, likely or probable carcinogens, and 48 pesticides flagged as potential endocrine (hormone) disruptors. More than 20 of the listed pesticides are classified as either extremely or highly hazardous by the World Health Organisation. Four pesticides are subject to actions by International Conventions but are still used in Australia - endosulfan, atrazine and diuron.

Pet cats and exposure to PBDEs
PBDEs are found in a wide range of manufactured products from televisions, computers and mobile phones to carpets, structural plastics, soft furnishings and curtains, but because of their characteristic failure to bind with plastic polymers, PBDEs can progressively leach into the environment. According to animal studies PBDEs are potent neuro-developmental toxins, disruptors of thyroid function and liver toxins. While the specific effects of the brominated flame-retardant PBDEs are beginning to be investigated, public health officials are taking interest in the now established association between low concentrations of PBDEs in laboratory and companion pet animals, and nervous system and reproductive effects, such as impaired learning and development, hyperthyroidism and cancer. A US EPA study published in August 2007 found hyperthyroidism had become one of the leading causes of death in pet cats in North America. Toxicologist and EPA veterinarian Janice Dye claimed that the increased incidence of hyperthyroid cats resulted from their prolonged contact with household plastics and that the meticulous grooming habits of cats caused them to ingest the PBBEs present in households.


 * "We definitely found evidence that cats are being exposed to these compounds based on the level of PBDEs in their blood. Cats are in a perfect position to be near the products these chemicals were put in to reduce flammability. Our results showed that cats are being consistently exposed to PBDE. Because they’re endocrine-disrupting agents, cats may well be at increased risk for developing thyroid effects." Dr Dye said.

The potential for diet to be a risk factor was also considered by researchers, and following their analysis of several commercially available cat food brands, the PBDE content of canned fish and foods with seafood flavours was significantly higher than dry or non-seafood canned items. As a result researchers estimated cats fed predominantly on a canned fish diet could have PBDE levels 12 times higher than those fed on dry food diets, and potentially be receiving as much as 100 times greater dietary PBDE intakes than American adult humans.

Obesity and chemical policy reform
In Tasmania, obesity and obesity related health problems are a major issue. As statistics presented in ‘Tasmanian State of Public Health Report 2008’ show, the prevalence of overweight and obesity (self-reported data) for 18 years and over, has jumped from 36.5% in 1989/90 to 48.9% in 2004/05. This is a significant increase. There are no figures for younger age groups and only the limited data from national surveys is available.

The report goes on to say with regard to obesity:

"Socio-environmental changes offer the best hope we have for addressing this socially-determined and major public health issue."

In the foreword of the report, Dr Roscoe Taylor, the Director for Population and Public Health, wrote:


 * "The collective approach spans all levels of government across a range of departments, non-government organisations, community groups, industry and employers, and benefits the entire population across the lifespan. Many of the best forms of public health promotion and protection are subtle or have become so accepted as part of our societal norms that they have become invisible, and go unsung. I commend such efforts to Parliament."

Beyond the simple sum of low socio-economic status, high alcohol and junk food intake and a sedentary lifestyle, some are also pointing to the role of environmental factors may be playing in the obesity epidemic. In September 2009 Newsweek reported that "early exposure to common chemicals may be programming kids to be fat." The report canvassed the possible role of 'obesogens', chemicals that can reprogramme cell development and metabolic rate.

Obesogens link the obesity epidemic directly to chemical contaminants. Preventative health strategies to reduce obesity and the ensuing burdening costly health problems must include a collective approach by all levels of government which in turn make chemical policy reform an essential ingredient of health care reform.

In April 2009 concerned doctors and scientists wrote to State ministers Lara Giddings and David Llewellyn specifically seeking a prohibition on the use and sale throughout the State of all pesticides which adversely affect health.

Related SourceWatch articles

 * Air pollution in Tasmania
 * Food quality in Tasmania
 * Landfill pollution in Tasmania
 * Marine pollution in Tasmania
 * Toxic heavy metals in Tasmania
 * Water pollution in Tasmania

External resources

 * "Natural Resources Defense Council" is a U.S.-based organisation that works to protect wildlife and wild places and to ensure a healthy environment for all life on earth.
 * "Pesticide Action Network" are an American based advocacy group that believe pesticides are a public health problem that requires public engagement to solve - they have publicly available information to help communities take action on pesticides.
 * "Environmental Health News" is a website that aims to advance the public’s understanding of environmental health issues by publishing its own journalism and providing access to worldwide news about a variety of subjects related to the health of humans, wildlife and ecosystems.
 * "Health and Environment Alliance" aims to raise awareness of how environmental protection and sustainability improves health and to empower the health community to contribute their expertise to policy making.
 * "US Environmental Protection Agency" registers or licenses pesticides for use in the United States and provides an insight into their regulatory system, including essential principles for reform of chemicals management legislation.
 * "Pesticides & Cancer" is website that hosts the The Sick of Pesticides campaign, which has been launched as part of a Europe-wide initiative to raise awareness of the links between pesticides and cancer.
 * "Collaborative on Health and the Environment" is a diverse network of more than 3000 individual and organizational partners in 45 countries and 48 states, working collectively to advance knowledge and effective action to address growing concerns about the links between human health and environmental factors. Regular newsletters are published on-line.
 * "The National Association for the Dually Diagnosed" is a environmental health project that provides a pesticides and mental health bibliography.

External articles

 * John Dudley, "Responding to the editorial Not weak on water", The Mercury, August 4, 2009.
 * Peter C Sims, "Toxic residues in food", The Mercury, August 4, 2009.
 * "EPA Pesticide Exposure Test Too Short, Overlooks Long Term Effects, According To Expert", Science Daily, August 17, 2009.
 * Heather Patisaul, "Atrazine acts in the brain to disrupt the hormones that trigger ovulation", Environmental Health News, August 20, 2009. (This is a synopsis of C.D. Foradori, L.R. Hinds, W.H. Hanneman and R.J. Handa, "Effects of atrazine on GnRH neuroendocrine function after its withdrawal in the adult female Wistar rat", Biology of Reproduction, 2009.)
 * Environmental Health Sciences, "Cancer in wildlife, normally rare, can signal toxic dangers", Environmental Health News, August 27, 2009.
 * Commission of the European Communities, "Communication of the Commission to the European Parliament, The Council, The European Economic and Social Committee and The Committee of Regions on Action Against Cancer: European Partnership", June 24, 2009.
 * Heather Hamlin & Wendy Hessler, "A bad mix: exposure may be “safe” only with one chemical at a time", Environmental Health News, September 1, 2009.
 * Richard Danielson, "Body of evidence shows that atrazine harms fish and amphibians, USF researchers say", St. Peterburg Times, October 1, 2009, sourced from tampabay.com.
 * Mark Johnson, "Children's diseases linked to chemicals on rise, professor says", Journal Sentinel, October 1, 2009.
 * ABC News, "Probe rules out cancer cluster at Hobart school", March 4, 2009.
 * Robina Suwol, "Embracing the Precautionary Principle by Robina Suwol", The Los Angeles Independent Media Center, July 27, 2009.
 * Farmers Weekly Interactive, "Brussels votes for pesticide clampdown", September 25, 2009.
 * Chris Wood, "NAFTA and the Unmanning of North America: A trade case with Canada highlights the evidence linking everyday products to the feminization and outright disappearance of males from every species — including ours", Miller McCune, March 3, 2009.
 * Joan Melcher, "Seeking Chemical Culprits for Those Deformities: Science casting wide net in search of chemicals seen as likely suspects in feminization and reproductive anomalies being spotted worldwide", Miller McCune, September 22, 2009.
 * Daily Mail, "Chemicals in breast milk linked to testicular cancer", Mail Online, September 25, 2009.
 * Take Action, "Endocrine disruptors disrupt common wisdom", Take Action Safer Chemicals Campaign, November 15, 2009. Short article about endocrine disrupting chemicals and how they impact on human health.
 * Science Daily, "Common Herbicides Block Important Nutrient Sensor in Humans", "Beyond Pesticides Website", October 15, 2009. Short article discussing how the use of common herbicides can lead to severe health risks.
 * Qinghua Sun, et al., "Ambient Air Pollution Exaggerates Adipose Inflammation and Insulin Resistance in a Mouse Model of Diet-Induced Obesity", "American Heart Association", January 19, 2009. Short article that shows a new link between air pollution and type 2 diabetes mellitus.